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Mar. Drugs 2014, 12(10), 5295-5315; doi:10.3390/md12105295

13-Acetoxysarcocrassolide Induces Apoptosis on Human Gastric Carcinoma Cells Through Mitochondria-Related Apoptotic Pathways: p38/JNK Activation and PI3K/AKT Suppression

1
Antai Medical Care Cooperation Antai Tian-Sheng Memorial Hospital, Pingtung 92842, Taiwan
2
Department of Beauty Science, Meiho University, Pingtung 91202, Taiwan
3
Department of Biotechnology, Kaohsiung Medical University, Kaohsiung, Taiwan
4
Graduate Institute of Applied Healthy and Biotechnology, Meiho University, Pingtung 91202, Taiwan
5
National Museum of Marine Biology and Aquarium, Pingtung 94446, Taiwan
6
Graduate Institute of Food Science, National Pingtung University of Science and Technology, Pingtung 91202, Taiwan
7
Department of Physical Medicine and Rehabilitation, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan
8
Department of Biomedical Sciences and Research Center for Emerging Viral Infections, College of Medicine, Chang Gung University, Taoyuan 33302, Taiwan
The authors contributed equally to this work.
*
Authors to whom correspondence should be addressed.
Received: 18 September 2014 / Revised: 15 October 2014 / Accepted: 20 October 2014 / Published: 23 October 2014
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Abstract

13-acetoxysarcocrassolide (13-AC), an active compound isolated from cultured Formosa soft coral Sarcophyton crassocaule, was found to possess anti-proliferative and apoptosis-inducing activities against AGS (human gastric adenocarcinoma cells) gastric carcinoma cells. The anti-tumor effects of 13-AC were determined by MTT assay, colony formation assessment, cell wound-healing assay, TUNEL/4,6-Diamidino-2-phenylindole (DAPI) staining, Annexin V-fluorescein isothiocyanate/propidium iodide (PI) staining and flow cytometry. 13-AC inhibited the growth and migration of gastric carcinoma cells in a dose-dependent manner and induced both early and late apoptosis as assessed by flow cytometer analysis. 13-AC-induced apoptosis was confirmed through observation of a change in ΔΨm, up-regulated expression levels of Bax and Bad proteins, down-regulated expression levels of Bcl-2, Bcl-xl and Mcl-1 proteins, and the activation of caspase-3, caspase-9, p38 and JNK. Furthermore, inhibition of p38 and JNK activity by pretreatment with SB03580 (a p38-specific inhibitor) and SP600125 (a JNK-specific inhibitor) led to rescue of the cell cytotoxicity of 13-AC-treated AGS cells, indicating that the p38 and the JNK pathways are also involved in the 13-AC-induced cell apoptosis. Together, these results suggest that 13-AC induces cell apoptosis against gastric cancer cells through triggering of the mitochondrial-dependent apoptotic pathway as well as activation of the p38 and JNK pathways. View Full-Text
Keywords: 13-acetoxysarcocrassolide; soft coral; gastric cancer cells; apoptosis; p38 and JNK pathways 13-acetoxysarcocrassolide; soft coral; gastric cancer cells; apoptosis; p38 and JNK pathways
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Su, C.-C.; Chen, J.Y.-F.; Din, Z.-H.; Su, J.-H.; Yang, Z.-Y.; Chen, Y.-J.; Wang, R.Y.; Wu, Y.-J. 13-Acetoxysarcocrassolide Induces Apoptosis on Human Gastric Carcinoma Cells Through Mitochondria-Related Apoptotic Pathways: p38/JNK Activation and PI3K/AKT Suppression. Mar. Drugs 2014, 12, 5295-5315.

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